Cardiovascular hypertension, NSAIDs

Some general principles for the treatment of Seronegative Spondylarthritis can be summarized as follows. Mild cases of SpA are controlled with physiotherapy and NSAIDs, paying attention to GI, renal, cardiovascular, hypertensive and hepatic risk... 

Selectivity for COX-1 versus COX-2 is variable and incomplete for the older NSAIDs, but many selective COX-2 inhibitors have been synthesized. The selective COX-2 inhibitors do not affect platelet function at their usual doses. In testing using human whole blood, aspirin, ibuprofen, indomethacin, piroxicam, and sulindac are somewhat more effective in inhibiting COX-1. The efficacy of -2-selective drugs equals that of the older NSAIDs, while gastrointestinal safety may be improved. On the other hand, selective COX-2 inhibitors may increase the incidence of edema and hypertension. As of December 2008, celecoxib and the less selective meloxicam are the only COX-2 inhibitors marketed in the USA. Rofecoxib and valdecoxib, two previously marketed, selective COX-2 inhibitors, have been withdrawn from the market due to their association with increased cardiovascular thrombotic events. Celecoxib has an FDA-initiated "black box" warning concerning cardiovascular risks. It has been recommended that all NSAID product labels be revised to include cardiovascular risks. 

The shift in hemostatic balance toward a prothrombotic state might not be the only mechanism by which COX-2 inhibitors could increase the risk of cardiovascular adverse effects. In fact, non-selective NSAIDs can raise blood pressure and antagonize the hypotensive effect of antihypertensive medications to an extent that may increase hypertension-related morbidity (55,56). The problem is clinically relevant, as arthritis and hypertension are common co-morbid conditions in elderly people, requiring concurrent therapy. 

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